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Flashcards in Structure - Function Deck (96)
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1

What is the cup shaped around the glomerulus

BOWMAN'S CAPUSULE

2

Smooth muscle cells found between / supporting glomerular capillaries, which can contract to regulate blood flow into the glomerulus.

They also have phagocytic properties similar to monocytes and release inflammatory cytokines and growth factors.

Mesangial Cells

3

What is special about the glomerular capillaries

They are fenestrated, and allow large amounts of solute-rich fluid (Ions and large molecules, not protein or blood cells) to pass through

They have podocytes - which make up the visceral epithelium of bowman's capsule

4

Where does the filtrate enter the (bowman's) capsular space

Filtration slits of the podocytes

5

Clefts between the foot processes of the podocytes

Filtration slits

6

Most nephrons are _____ They are the "hard workers" and have a shorter loop of henle

Cortical Nephrons

7

About 15% of nephrons are ______ They have a long loop of henle

Juxtaglomerular Nephrons

8

What do juxtaglomerular nephrons specialize in

CONCENTRATING URINE

9

Where does renal filtration occur?

Glomerulus

10

Where does renal reabsorption and secretion occur?

Tubules

11

Name the two kinds of capillaries found in nephrons

Glomerular - filtration!

Peritubular -

12

The only capillaries in the body that are fed and drained by an arteriole

Glomerular capillaries

13

When filtrate reabsorbed by the tubules, how does it return to the blood stream

via peritubular capillaries

14

What allows the blood pressure in the glomerular capillary bed to be so high?

The fact that these glomerular capillaries are fed and drained by an arteriole

15

On what forces does glomerular filtration depend

STARLING forces - hydrostatic and osmotic pressures

16

What makes glomeruli efficient filters?

1. large surface area
2. Surface is very permeable to water
3. High glomerular BP (55 mmHg) (higher than capsule pressure)

17

Glomerular BP?

55mmHg

18

What opposes glomerular filtration?

Osmotic pressure in the plasma from protein

Fluid pressure in Bowman's space

1. Increase plasma protein (dehydration, polycythemia)
2. Increase BS pressure
3. Decrease BP

19

What favors glomerular filtration?

Glomerular capillary BP

1. raise systemic BP
2. Decrease pressure in BS
3. Decrease plasma protein (blood loss, no transfusion)

20

Tubular cells are joined by _____ through which substances can _______

Tight junction, diffuse

21

Percentage of urea reabsorbed

44%

22

Percentage of Na reabsorbed

99.5%

23

Percentage of water reabsorbed

99%

24

Examples of things which are secreted in the tubules

H+

K+

Organic anions

25

Tubule secretion is particularly important for which homeostatic mechanism

Controlling blood pH (H+ secretion)

26

Normal GFR

90/120 ml/min

< 60 = disease

27

GFR affected by

1. Filtration surface area
2. Membrane permeability and Net Filtration Pressure (NFP)
3. Blood pressure / flow to glomerulus

28

Key mechanisms kidneys use to regulate water and ions

Water reabsorption

Na reabsorption / secretion

29

Range of daily urine volume

400 - 2500mL

30

Renal salt wasting

Hypo-aldosteronism

31

Order of operations in nephron

Afferent arteriole > glomerulus > Prox convoluted tubule > Descending loope of henle > Loop > thin ascending loop > thick ascending loop > distal convoluted tubule > (cortex, medulla) > Collecting duct > papilla of renal pyramid > minor and major calyces >renal pelvis (Hilum) > Ureter

32

What makes up the renal corpuscle

Glomerulus, bowman's capsule, mesangial cells

33

Major disorders that disrupt the glomerular filtration barrier

DMII, HTN, Glomerulonephritis (autoimmune)

34

Where does sodium reabsorption occur and how is it transported?

Occurs in all tubular segments EXCEPT the descending loop of Henle (for the countercurrent!)

Transported passively, by diffusion, from the tubular lumen to the epithelial cells. Then transported actively, via Na/K pump, from the epithelial cells to the systemic capillaries

35

By what mechanism is water reabsorbed

Osmosis (passive) - but ** determined by the movement of sodium and presence of aquaporins **

36

Sites for water / Na balance

Renal Tubules

37

Where would one find aquaporins?

Proximal convoluted tubule +++

Descending, loop, ascending?

NONE in collectinge ducts UNLESS YOU HAVE ADH

38

ADH is produced where and alongside what?

Produced in HYPOTHALAMUS

STORED in POSTERIOR PITUITARY

alongside oxytocin

39

How does ADH lead to increased aquaporins

increased plasma osmolarity > ADH from post pituitary >
binds receptors on basolateral membrane of COLLECTING DUCTS >
increased cAMP / PO4 >
AQP fuse w luminal membrane

40

How is sodium transported in renal tubules?

Transported passively, by diffusion, from the tubular lumen to the epithelial cells.

Then transported actively, via Na/K pump, from the epithelial cells to the systemic capillaries

41

Why is active transport of Na out of the tubule epithelial cells necessary?

To keep intracellular Na low and drive the diffusion gradient

42

Things which might disrupt the homeostasis of passive / active Na reabsorption and subsequent H20 / glucose drafting?

Broken AQPs

Lack of ATP in kidney

Tubular damage w interstitial fibrosis

43

How to baroreceptors in the atria and carotid arteries affect ADH

Lower BP at carotid / atrial baroreceptors will inhibit ADH, so the kidneys will hold on to water and increased blood volume / BP

44

How does SIADH affect fluid homeostasis

1. Too much ADH > too much water reabsorbed / retained
2. High BP, low Na

45

How does Diabetes Insipidus affect fluid homeostasis?

1. Not enough or ineffective ADH
2. Low BP, high Na
3. Large, dilute volumes urine

46

Where does concentration of urine happen/

Loop of Henle

47

What special function does the special structure of the loop of henle provide?

Countercurrent Multiplier

48

Osmolarity of filtrate in proximal tubule and beginning of descending loop vs plasma

IT'S THE SAME IT'S THE SAME

49

Describe how the osmolarity of filtrate changes throughout the tubules

PCT and beginning of descending loop (same as plasma)

Osmolarity increases (concentration) as filtrate travels down the descending limb - because only water is reabsorbed here. Impermeable to solutes.

Osmolarity decreases (dilutes) as filtrate travels up the ascending limb - because Na is reabsorbed. Permeable to solutes.

Filtrate entering the DCT is very dilute - as low as 70mOsm

Osmolarity either increases, decreases, or stays the same as filtrate travels down collecting duct - depending on body's needs, presence of ADH etc

50

What contributes to the medullary osmotic gradient

Urea recycling

51

How dilute can filtrate be by the time it reaches the DCT ?

Very dilute - as low as 70mOsm

52

How concentrated can urine become?

1200 mOsm

53

Key controller of Na reabsorption?

Aldosterone

54

Aldosterone site / action

Steroid, from adrenal cortex

Increases Na reabsorption from distal tubules and collecting ducts

** fine- tuning here - bulk reabsorption already happening in earlier tubules **

55

Increases Na reabsorption from distal tubules and collecting ducts by dumping K

Aldosterone

Hold Na, at the expense of K

56

JGA consists of

JG cells + Macula Densa

57

Enlarged, specialized smooth muscle cells that secrete renin and control blood flow to glomerulus

JG cells

58

Are JG cells considered endocrine?

YES

59

What kind of receptors to JG cells use to detect BP shifts in afferent arteriole?

Mechanoreceptors

60

How to renin and aldosterone relate?

JG cells detect Low BP > JG cells secrete Renin > Angiotensinogen / I / II > Aldosterone

61

A group of tall, closely packed cells in the DCT which detect changes in Na / osmolarity via chemoreceptors

Macula Densa

62

What does low Na in the DCT mean for Macula Densa?

Low Na = decreased filtration >> JG cells release renin (Paracrine signaling!!)

63

What controls aldosterone?

Renin, Angiotensin II >>
Adrenal Cortex >
Aldosterone >
Na and H20 retention

64

Three triggers for Renin release

1. Low BP (JGA, less stretch = more renin)
2. Low Na (Macula)
3. SNS stimulation (JG)

65

Atrial Natriuretic Peptide and Na

Increased BP > cardiac distention > ANP released

ANP > decreased aldosterone > Na dumped
ANP > afferent dilation, efferent constriction > Increased GFR

66

Major extracellular buffering system

CO2 / HCO3 system

67

Major intracellular buffers

Phosphate and proteins

68

How do the kidney's alter the body's pH?

By altering the plasma HCO3 concentration

HCO3 is filtered, then reabsorbed or secreted in tubules according to body's pH needs

Normally, all filtered HCO3 is "reabsorbed" (H exchange mechanism)

69

A "low oxygen" environment, this area of the kidney is particularly prone to ischemia

Medulla!

70

The structure of this area makes it particularly vulnerable to deposition of immune complexes, compliment fixation, and damage from HTN and glycosylation

Glomerulus!

(highly vascular, fenestrated structure)

71

This area gets clogged by things that shouldn't have made it through the glomerulus and is therefore prone to ischemia

Tubules!

RBC, WBC, Protein, Fat, Stones

72

These structures are more prone to malformation, obstruction, and masses

"Post renal" structures - ureters, bladder

73

Renal medulla is particularly prone to what kind of problem

Ischemia

74

Glomerulus is particularly prone to what kinds of problems

Due to fenestrated vasculature:

Deposition of immune complexes, complement
HTN damage
Glycosylation

75

Tubules are particularly prone to

Ischemia, clogged by large molecules that make it through damaged glomeruli (WBC, RBC, protein etc)

76

Post renal structures are particularly prone to what kinds of problems

Malformation
Obstruction
Masses

77

What "pre renal" structures can cause renal problems?

Vascular - Renal Artery

General blood volume / perfusion

DRUGS (NSAIDs, ACEi, diuretics)

78

Heterogenous group of disorders characterized by rapid deterioration of renal function (GFR), rapid elevation of BUN, and S Cr, oliguria

ACUTE renal failure

79

Acute Renal Failure, Pre-renal causes (30%)

CV, volume depletion (ischemia)

Drug induced (NSAIDs, ACE, diuretics)

80

Acute Renal Failure, Intrarenal causes (60%)

Inflammatory diseases

Acute Tubular Necrosis

81

Acute Renal Failure, Post Renal causes (10%)

OBSTRUCTION

Cancer

Congenital abnormalities

82

60% of acute renal failure is caused by

Intrarenal problems, mostly Acute Tubular Necrosis

*ATN, when blood supply to kidney is severely reduced or blocked. Tubular cells slough off and form casts

83

30% of acute renal failure is caused by

Pre renal, hemodynamic

84

10% of acute renal failure is caused by

Post renal, OBSTRUCTION

85

Slow, progressive loss of renal function associated with:

Systemic diseases (HTN, DM, SLE) or

Intrinsic kidney disease (kidney stones, acute kidney injury, chronic glomerulonephritis, chronic pyelonephritis, obstructive uropathies, or vascular disorders)

Chronic Kidney Disease

86

Clinical definition of CKD

GFR less than 60 ml/min/1.73 m2 for 3 months or more
Irrespective of the initial cause of the renal damage

87

Anatomical changes to kidney in CKD

Granular surface
Smaller size

Decreased function
high urine protein

88

Stage 1 CKD

GFR > 90

No obvious disease. GFR being compensated by higher kidney pressure

89

Stage 2 CKD

GFR 60-89

Early evidence of bone disease (VD3)
Creeping SrCr
EPO anemia
Mild HTN

90

Stage 3 CKD

GFR 30-59

Elevated SrCr and Urea
Mod HTN
High Triglycerides
Metabolic Acidosis

91

Stage 4 CKD

GFR 15-29

Hyperkalemia
Na / H2O retention
Increasing SrCr / Urea

92

Stage 5 CKD

GFR 0-14

Significant Uremia
Death

93

GFR for Kidney Failure

< 15

94

When do symptomatic changes appear in renal failure

Not until renal function declines to < 25% of normal (75% loss) - when adaptive reserves have bee exhausted

95

What causes the symptoms of renal failure

Symptoms result from:
increased levels of creatinine, urea, and potassium

alterations in salt and water balance

96

Intact nephron hypothesis

when nephrons are lost, the surviving nephrons step up their game to sustain normal kidney function